• Biomedical Science Letters
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• v.14 no.3
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• pp.131-137
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• 2008

Adipogenesis is a complex sequence of events that culminates in the differentiation of fibroblast-like preadipocytes into specialized lipid-filled adipocytes and also involves a cascade of expression of many transcription factors such as peroxisome proliferator-activated receptor ${\gamma}(PPAR{\gamma})$ and CCAAT/enhancer-binding proteins (C/EBPs). $PPAR{\gamma}$ and C/EBPs transcriptionally transactivate adipocyte specific genes, including fatty acid transport protein (FAT/CD36) and leptin. To determine whether $17{\beta}$-estradiol modulates $C/EBP{\alpha}$ actions on adipogenesis in high fat diet-fed female ovariectomized (OVX) C57BL/6 mice, mice were treated with $17{\beta}$-estradiol for 7 days and the effects of $17{\beta}$-estradiol on adipose tissue mass and expression of adipocyte specific gene as well as $C/EBP{\alpha}$ were measured. Compared to vehicle-treated OVX control mice, OVX mice treated with $17{\beta}$-estradiol for 7 days had lower adipose tissue weights that were similar to weights in high fat diet-fed sham-operated (Sham) mice. OVX mice showed the increased expression of $C/EBP{\alpha}$ mRNA compared with Sham mice. However, $17{\beta}$-estradiol treatment in OVX mice inhibited OVX induced-$C/EBP{\alpha}$ activation, indicating that $17{\beta}$-estradiol may act as an inhibitor of $C/EBP{\alpha}$ action. Moreover, $17{\beta}$-estradiol decreased mRNA levels of adipocyte marker genes, such as lipoprotein lipase, FAT/CD36 and leptin, to levels in Sham mice. These results suggest that down-regulation of adipogenesis by $17{\beta}$-estradiol may be due to reduced adipose $C/EBP{\alpha}$ activities in female OVX C57BL/6 mice.

• IMMUNE NETWORK
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• v.8 no.3
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• pp.90-97
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• 2008

Background: Hypersensitivity pneumonitis (HP) comprises a group of lung diseases resulting from repeated inhalation of various antigens such as Saccharopolyspora rectivirgula (SR). HP is categorized as a Th1 disease. Therefore, it has been suggested that IL-4, Th2 type cytokine, plays a protective role in the development of HP. However, the functional role of IL-4 in HP has not been extensively investigated in vivo. Therefore, we investigated the functional role of IL-4 in HP using IL-4 knockout (KO) mice. Methods: HP was induced by repeated exposure to SR in C57BL/6 (B6) and IL-4 KO (C57BL/6 background) mice. Results: IL-4 KO mice aggravated HP in terms of histological alteration, SR-specific immune responses, and inflammatory cell infiltration in the lungs compared with B6 mice. IL-4 KO mice produced high levels of IFN-${\gamma}$, TGF-${\beta}$ and TNF-${\alpha}$ in the lungs, whereas B6 mice showed the enhanced production of IL-4. Moreover, chemokines such as MIP-1${\alpha}$, MCP-1, and RANTES were highly expressed in IL-4 KO mice. IFN-${\gamma}$-secreting CD4, CD8 T cells, and neutrophils were enhanced in the bronchoalveolar lavage fluid (BALF) of IL-4 KO mice than those of B6 mice. The administration of recombinant(r) IL-4 restored these immunologic parameters in IL-4 KO mice. Conclusion: These results indicate that IL-4 plays a suppressive role in SR-induced HP by attenuating Th1-dominant immune responses.

• Toxicological Research
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• v.29 no.1
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• pp.7-14
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• 2013

Betaine supplementation has been shown to alleviate altered glucose and lipid metabolism in mice fed a high-fat diet or a high-sucrose diet. We investigated the beneficial effects of betaine in diabetic db/db mice. Alleviation of endoplasmic reticulum (ER) and oxidative stress was also examined in the livers and brains of db/db mice fed a betaine-supplemented diet. Male C57BL/KsJ-db/db mice were fed with or without 1% betaine for 5 wk (referred to as the db/db-betaine group and the db/db group, respectively). Lean non-diabetic db/+ mice were used as the control group. Betaine supplementation significantly alleviated hyperinsulinemia in db/db mice. Betaine reduced hepatic expression of peroxisome proliferator-activated receptor gamma coactivator 1 alpha, a major transcription factor involved in gluconeogenesis. Lower serum triglyceride concentrations were also observed in the db/db-betaine group compared to the db/db group. Betaine supplementation induced hepatic peroxisome proliferator-activated receptor alpha and carnitine palmitoyltransferase 1a mRNA levels, and reduced acetyl-CoA carboxylase activity. Mice fed a betaine-supplemented diet had increased total glutathione concentrations and catalase activity, and reduced lipid peroxidation levels in the liver. Furthermore, betaine also reduced ER stress in liver and brain. c-Jun N-terminal kinase activity and tau hyperphosphorylation levels were lower in db/db mice fed a betaine-supplemented diet, compared to db/db mice. Our findings suggest that betaine improves hyperlipidemia and tau hyperphosphorylation in db/db mice with insulin resistance by alleviating ER and oxidative stress.

• The Journal of the Korea Contents Association
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• v.20 no.3
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• pp.506-514
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• 2020

The purpose of this paper is to examine the factors influencing usage intentions of Social Network Services (SNS) in MICE (Meeting, Incentive travel, Convention, and Exhibit and Event) and moderating effects of gender. This model tests various theoretical research hypotheses relating to MICE industry, SNS characteristics, and Technology Acceptance Model (TAM). The target population of this study is SNS users with MICE participation experience. The results of hypothesis testing are as follows. First, information provision, convenience, service quality and SNS usage experience positively influence attitudes toward SNS. Second, attitude positively influences usage intention of SNS. Finally, information provision and service quality to attitudes toward SNS for males are significantly large than those for females. Convenience and SNS usage experience to attitudes toward SNS for females are significantly large than those for males. And attitude to usage intention toward SNS for males are significantly large than those for females. The results of this study will provide various implications to improve usage intentions of SNS in MICE industry.

• Clinical and Experimental Reproductive Medicine
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• v.47 no.1
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• pp.20-33
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• 2020

Objective: The differences between type 1 and type 2 diabetes mellitus (T1DM and T2DM) in terms of their adverse effects on male reproductive parameters have never been elucidated. This study aimed to distinguish between the effects of the DM types in mice treated with multiple low doses of streptozotocin (STZ) to mimic human T1DM and coadministered a high-fat diet (HFD) to mimic human T2DM. Methods: The T1DM mice were intraperitoneally injected with STZ (40 mg/kg body weight) for 5 days. The T2DM mice received an HFD for 14 days prior to STZ injection (85 mg/kg body weight), followed by continuous feeding of an HFD. Male reproductive parameters were evaluated. Results: The reproductive organs of the DM mice weighed significantly less than those of controls, and the seminal vesicles plus prostates of the T1DM mice weighed less than those of the T2DM mice. Increased sperm abnormalities and incomplete DNA packaging were observed in the DM groups. Sperm concentration and the proportion of normal sperm were significantly lower in the T1DM group. The seminiferous histopathology of DM mice was classified into seven types. The penises of the DM mice were smaller than those of the controls; however, tunica albuginea thickness and the amount of penile collagen fibers were increased in these mice. Round germ cells were abundant in the epididymal lumens of the mice with DM. Conclusion: T1DM adversely affected reproductive parameters to a greater extent than T2DM.

• Parasites, Hosts and Diseases
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• v.25 no.2
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• pp.199-208
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• 1987

The chemotherapeutic efficacy of trimethoprim-sulfamethoxazole ($Bactrim^{\circledR}$) in mice experimentally infected with Toxoplasma gcndii was evaluated. The average survival days and survival rate of mice infected intraperitoneally with $1{\times}10^5$ trophozoites and treated with $Bactrim^{\circledR}$ were compared with those of untreated group. The hematologic findings of blood samples of experimental mice were observed for comparison of side elects between $Bactrim^{\circledR}$ and pyrimethamine ($Daraprim^{\circledR}$), the latter of which has been one of the favorable drugs for the treatment of toxoplasmosis. The results are summarized as follows: 1. $Bactrim^{\circledR}$ showed a strong evidence of potent anti-Toxoplasma activity. The survival rate of mice administered with 24 mg of $Bactrim^{\circledR}$ per mouse per day for 7 days, was 83.3%, and the rate was increased to 100% in mice administered with two-fold concentrated dose of the drug. 2. The average numbers of white blood cells (W.B.C.) in the mouse groups treated with $Bactrim^{\circledR}$ or $Daraprim^{\circledR}$ were more increased than those only infected with T. gondii. The mice treated with $Daraprim^{\circledR}$ however, showed remarkably decreased numbers of W.B.C. as compared with those treated with $Bactrim^{\circledR}$ . 3. The average numbers of red blood cells (R.B.C.) and platelets both in the drug-treated and untreated T. gondii-infected mice were decreased as compared with normal mice. The numbers of R. B. C. in $Daraprim^{\circledR}-treated$ mice, however, were more decreased than in $Bactrim^{\circledR}-treated$ mice. 4. The average levels of hemoglobin both in the drug.treated and untreated T. gondii-infected mice were decreased, compared with normal mice. But there was no difference in the levels of hemoglobin between $Bactrim^{\circledR}$ and $Daraprim^{\circledR}-treated$ groups. In conclusion, trimethoprim.sulfamethoxasole ($Bactrim^{\circledR}$) was proven to be effective and safe for the treatment of murine toxoplasmosis. The efficacy was comparable with pyrimethamine ($Daraprim^{\circledR}$), but bone marrow depression was less severe with $Bactrim^{\circledR}$ treatment.

• YAKHAK HOEJI
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• v.44 no.5
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• pp.391-398
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• 2000

Leptin, the product of the ob gene, is a small peptide molecule synthesized by white adipocytes with an important role in the regulation of body fat and food intake. Based on the evidence that synthesis of leptin is regulated by female sex hormone, estrogen, this present study was investigated whether sex hormone precursor DHEA, can regulate obese gene expression in lean and genetically obese (ob/ob) mice. Antiobesity activity of DHEA was evaluated by determining body weight, food consumption, epididymal fat weight and serum levels of cholesterol and triglyceride in ICR, C57BL/6J, and ob/ob mice. The treatment of C57BL/6J lean and obese mice with a diet containing 0.3% and 0.6% DHEA resulted in lowered rates of weight gain in comparison to non-treated mice, although much greater response was found in the obese mice. All other concentrations of DHEA (0.015%, 0.06%, 0.15%, 0.3%) except the highest one(0.6%) showed no significant effects on weight gain in ICR mice. Food consumption was significantly decreased in all mice treated with 0.6% DHEA, whereas it was not decreased in ICR mice at lower concentrations than 0.6% DHEA. DHEA decreased significantly epididymal adipose tissue weight and serum triglyceride levels dose dependently in lean and obese mice. However serum cholesterol levels were decreased at lower concentrations than 0.15% DHEA and increased at concentrations of 0.3% and 0.6% DHEA in lean and obese mice. These increases in serum cholestrol levels at high concentrations of DHEA might result from the fact that DHEA has a cholesterol moiety thereby interfered the assay system. As an approach to elucidate the mechanism for antiobesity activity of DHEA, we examined mRNA levels of obese gene in the adipocyte and obese gene product (leptin) in the serum. The results showed that DHEA did not affect obese gene expression in ICR and C57BL/6J mice. Therefore, we concluded that antiobesity activity of DHEA was not modulated by obese gene expression.

• Biomedical Science Letters
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• v.11 no.3
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• pp.259-266
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• 2005

Mast cells and goblet cells have been known to protect the host against parasites. In this study, we examined the response of the mast cells and goblet cells over a period of 6 weeks in the duodenum, jejunum and ileum of C3H/HeN and C57BL/6 mice infected with Echinostoma hortense (E. hortense). In addition, we investigated whether the worm recovery rate of uninfected mice (the control group) or E. hortense-infected mice (the experimental group) was associated with the number of mast cells and goblet cells. The worm recovery rate was higher in the C3H/HeN mice than in the C57BL/6 mice. The number of goblet cells significantly increased in the experimental group of the C3H/HeN and C57BL/6 mice compared with the control group of both strains (P<0.005). Worm recovery peaked 3 weeks after the infection of the C57BL/6 mice and at 2 weeks after the infection of the C3H/HeN mice, and it was higher in the duodenum than in the jejunum and ileum. However, the infected site in the intestine had no relation with worm expulsion. In the C3H/HeN and C57BL/6 mice, the number of goblet cells in the experimental group was significantly higher than that in the control group (P<0.005). The number reached a peak 2 weeks after the infection and it even increased in duodenum, jejunum and ileum. The increased number of goblet cells was retained 6 weeks after infection. The number of goblet cells was higher in the C3H/HeN mice than in the C57BL/6 mice (P<0.01). These results indicate that goblet cells are related with the worm expulsion. Furthermore, immunohistostaining of the antral intestinal walls for lectin showed the significant increase of the number of goblet cells in the experimental group (P<0.001). The high infection rate in the duodenum was found during the early infection. An increased infection rate in the jejunum and ileum was found 3 weeks after infection and the infection rate was higher in the C3H/HeN mice than in the C57BL/6 mice. Taken together, the present study indicates that goblet cells, rather than mast cells, may play critical roles in parasite expulsion.

• Biomedical Science Letters
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• v.9 no.3
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• pp.145-150
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• 2003

In the intestinal mucosa, mast cells are thought to be responsible for the expulsion of parasites. We investigated the relationship of worm expulsion and mast cells in C3H/HeN and BALB/c mice infected with Echinostoma hortense. In addition, we examined whether the worm recovery rate was associated with the strain of mice, and whether a toluidine stain and immunohistochemistry using the c-kit antibody was effective in the detection of mast cells. In order to investigate the mucosal immune response of C3H/HeN and BALB/c mice, each mouse was infected orally with 30 E. hortense metacercariae. Then, the number of mucosal mast cells and worm recovery rates was observed in experimentally infected mouse strains between 1 week and 8 weeks post infection (PI). Mucosal mast cells were increased in 3 weeks P.I. in C3H/HeN and BALB/c mice. On the other hand, only mucosal goblet cells and worm recovery rates correlated in C3H/HeN mice (P=0.0482). Worm recoveries in C3H/HeN mice were 65.7$\pm$5.6, 53.3$\pm$5.4 and 6.7$\pm$0.6 in week 1, 2, and 3 P.I. and strongly decreased in week 3 P.I. Worm recoveries in BALB/c mice were 23.0$\pm$2.5, 10.0$\pm$1.0, and 6.7$\pm$0.6% in week 1, 2, and 3 P.I. and gradually decreased from week 1 P.I. to week 3 P.I. Worm recoveries in C3H/HeN mice were significantly higher than in BALB/c mice (P<0.00l). The number of mast cells in C3H/HeN and BALB/c mice using the anti-c-kit antibody reached to a peak in week 3 P.I. and recovered as normal level in week 5 P.I. and 6 P.I. The number in E. hortense-infected C3H/HeN mice (P=0.0015) was higher than in E. hortense-infected BALB/c mice (P=0.01) compared with the control group. There were significant differences in the number of mast cells among regions of the intestine in in C3H/HeN mice (P<0.05) but not in BALB/c mice (P>0.05). Immunohistochemistry using the anti-c-kit antibody was significant method as an examination of the number of mast cells (P=0.0002). In conclusion, the present study demonstrated that mast cells play an important role in worm recovery, and immunohistochemistry using the anti-c-kit antibody was superior to toluidine stain as an examination of mast cells.

• Proceedings of the Korean Society of Toxicology Conference
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• 2000.11a
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• pp.45-67
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• 2000

2-Amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) is a mutagenic and carcinogenic heterocyclic amino found in cooked meat. The in vivo mutagenicity and hepatocarcinogenicity of MeIQx were examined in mice harboring the lacZ mutation reporter gene ($Muta^{TM}$ Mice) and bitransgenic mice over-expressing the c-myc oncogene. C57B1/$\lambda$lacZ and bitransgenic c-myc (albumin promoter)/$\lambda$lacZ mice were bred and weaned onto an AIN-76 based diet containing $0.06\%$ (w/w) MeIQx or onto control diet. After 30 weeks on diet, only male bitransgenic mice on MeIQx developed hepatocellular carcinoma ($100\%$ incidence) indicating that there was synergism between c-myc over-expression and MeIQx. By 40 weeks, hepatic tumor incidence was $100\%$ ($17\%$) and $44\%$ ($0\%$) in male c-myc/$\lambda$lacZ and C57B1/$\lambda$lacZ mice given MeIQx (or control) diet, respectively, indicating that either MeIQx or c-myc over-expression alone eventually induced hepatic tumors. At either time point, mutant frequency in the lacZ gene was at least 40-fold higher in MeIQx-treated mice than in control mice of either strain. These findings suggest that MeIQx-induced hepatocarcinogenesis is associated with MeIQx-induced mutations. Elevated mutant frequency in MeIQx-treated mice also occurred concomitant with the formation of MeIQx-guanine adducts as detected by the $^{32}P$-postlabeling assay. Irrespective of strain or diet, sequence analysis of the lacZ mutants from male mouse liver showed that the principal sequence alteration was a single guanine-base substitution. Adenine mutations, however, were detected only in animals on control diet. MeIQx-fed mice harboring the c-myc oncogene showed a l.4-2.6-fold higher mutant frequency in the lacZ gene than mice not carrying the transgene. Although there was a trend toward higher adduct levels in c-myc mice, MeIQx-DNA adduct levels were not significantly different between c-myc/$\lambda$lacZ and C57B1/$\lambda$lacZ mice after 30 weeks on diet. Thus, it appeared that factors in addition to MeIQx-DNA adduct levels, such as the enhance rate of proliferation associated with c-myc over-expression, may have accounted for a higher mutant frequency in c-myc mice. In the control diet groups, the lacZ mutant frequency was significantly higher in c-myc/$\lambda$lacZ mice than in 057B1/$\lambda$1acZ mice. The findings are consistent with the notion that c-myc over-expression is associated with an increase in mutagenesis. The mechanism for the synergistic effects of c-myc over-expression on MeIQx hepatocarcinogenicity appears to involve an enhancement of MeIQx-induced mutations.